Key result
Combined worsening renal function and higher rank of tubular injury in chronic heart failure patients was associated with a significantly increased risk of adverse clinical events (HR 15.0; 95% CI 2.0-111.0).
Why the study?
It was uncertain whether chronic heart failure patients are susceptible to renal tubular damage alongside worsening renal function preceding clinical outcomes.
Do changes in tubular damage biomarkers and worsening renal function predict clinical outcomes in patients with chronic heart failure?
Cohort (n=263)
Do changes in tubular damage biomarkers and worsening renal function predict clinical outcomes in patients with chronic heart failure?
Trajectories of tubular damage biomarkers and worsening renal function have different clinical determinants but both independently and additively predict adverse clinical outcomes in chronic heart failure.
May support combined renal assessment for risk stratification in chronic HF; hypothesis-generating and requires prospective validation.
Background It is uncertain that chronic heart failure (CHF) patients are susceptible to renal tubular damage with that of worsening renal function (WRF) preceding clinical outcomes. Hypothesis Changes in tubular damage biomarkers are stronger predictors of subsequent clinical events than changes in creatinine (Cr), and both have different clinical determinants. Methods During 2.2 years, we repeatedly simultaneously collected a median of 9 blood and 8 urine samples per patient in 263 CHF patients. We determined the slopes (rates of change) of the biomarker trajectories for plasma (Cr) and urinary tubular damage biomarkers N‐acetyl‐β‐ d ‐glucosaminidase (NAG), and kidney‐injury‐molecule (KIM)‐1. The degree of tubular injury was ranked according to NAG and KIM‐1 slopes: increase in neither, increase in either, or increase in both; WRF was defined as increasing Cr slope. The composite endpoint comprised HF‐hospitalization, cardiac death, left ventricular assist device placement, and heart transplantation. Results Higher baseline NT‐proBNP and lower eGFR predicted more severe tubular damage (adjusted odds ratio, adj. OR [95%CI, 95% confidence interval] per doubling NT‐proBNP: 1.26 [1.07‐1.49]; per 10 mL/min/1.73 m 2 eGFR decrease 1.16 [1.03‐1.31]). Higher loop diuretic doses, lower aldosterone antagonist doses, and higher eGFR predicted WRF (furosemide per 40 mg increase: 1.32 [1.08‐1.62]; spironolactone per 25 mg decrease: 1.76 [1.07‐2.89]; per 10 mL/min/1.73 m 2 eGFR increase: 1.40 [1.20‐1.63]). WRF and higher rank of tubular injury individually entailed higher risk of the composite endpoint (adjusted hazard ratios, adj. HR [95%CI]: WRF 1.9 [1.1‐3.4], tubular 8.4 [2.6‐27.9]; when combined risk was highest 15.0 [2.0‐111.0]). Conclusion Slopes of tubular damage and WRF biomarkers had different clinical determinants. Both predicted clinical outcome, but this association was stronger for tubular injury. Prognostic effects of both appeared independent and additive.
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Branković et al. (2020) conducted a cohort in Chronic heart failure (n=263). Worsening renal function and tubular injury vs. No worsening renal function or tubular injury was evaluated on Composite of HF-hospitalization, cardiac death, left ventricular assist device placement, and heart transplantation (HR 15.0, 95% CI 2.0-111.0). Combined worsening renal function and higher rank of tubular injury in chronic heart failure patients was associated with a significantly increased risk of adverse clinical events (HR 15.0; 95% CI 2.0-111.0).
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